Numerous studies have demonstrated that salicylic acid (SA), jasmonic acid (JA) and ethylene play key roles in activation of various defense responses following pathogen attack. Induction of SA-mediated responses occurs via both NPR1- dependent and -independent pathways. The SA- and JA/ethylene-mediated pathways appear to be coordinately regulated with extensive cross-talk occurring between them. The nature of this cross-talk is poorly understood and may involve complex regulatory mechanisms. In addition, environmental factors can significantly and sometimes dramatically influence the outcome of plant-pathogen interactions; the molecular and cellular basis for these effects is largely unknown. Two groups of Arabidopsis mutants have been isolated whose initial characterization argues that they will provide important insights into the molecular mechanisms underlying (i) the NPR1- dependent vs -independent pathway(s), (ii) the cross-talk between the SA- and JA/ethylene- mediated pathways and (iii) the effects of environment on disease resistance. The discovery that the fatty acid 18:1, or a derivative of it, functions as a signal together with JA to activate expression of the defensin gene PDF1.2, but suppresses SA-dependent defense response is particularly exciting. This co-activating signal was uncovered in the ssi2 mutant. ssi2 suppresses salicylate insensitivity of the npr1-5 mutant due to a mutation in a stearoyl-ACP desaturase which results in reduced fatty acid desaturation. One of the highest priorities is to determine whether 18:1 itself, or rather a derivative of it, is the co-activating signal. Suppressor mutants of ssi2 will also be isolated in order to better characterize the co-activating signal and its role in modulating defense responses. The genes for two other ssi mutants, ssi1 and ssi4, have been cloned. In addition to isolating suppressors of each, it will be determined whether the function of other genes shown to have a role in SA signaling (ed. PAD3 or PAD4), JA/ ethylene signaling (eg. COI1 or ETR1) or R gene-mediated signaling (eg. NDR1 or EDS1) are required for some or all of the mutant phenotypes. The second group of mutants constitutively expresses pathogenesis-related genes (cpr). cpr22, also exhibit SA-dependent (i) lesion formation, (ii) enhanced disease resistance and (iii) homozygous lethality as well as JA/ ethylene-mediated constitutive PDF1.2 gene expression. Interestingly, the SA -dependent, but not JA-mediated, phenotypes are suppressed by high relative humidity (RH). High RH also suppresses the SA-dependent phenotype of ssi4. In addition, ssi4 is extremely cold sensitive, with death occurring at 16 degrees C. Thus, further characterization of cpr22 and ssi4 by conducting epistatic analyses and/or isolating suppressor mutants for each of these pathways should provide valuable insights into how environmental factors (RH and temperature) influence disease resistance. It should be noted that SA may also play a signaling role in other processes, including thermogenesis, cell growth and trichome development. Thus, elucidation of the components involved in the SA defense signaling pathways may well provide insights into a much larger signaling network through which plants regulate a wide variety of responses.
